Self-reported weight and height: implications for left ventricular hypertrophy detection. An Italian multi-center study

We examined the difference between self-reported and measured body size values and their impact on detection of left ventricular hypertrophy (LVH) by echocardiographic LV mass indexation. A total of 1963 subjects referred by their practitioners for routine echocardiographic examination to nine outpatient echocardiographic laboratories across Italy were included in the study. Left ventricular hypertrophy was defined according to two gender- specific criteria as: A) Left ventricular mass (LVM) index ≥49 g/h(2.7) in men and ≥45 g/h(2.7) in women; B) LVM index ≥125 g/m(2) in men and ≥110 g/m(2) in women. Prevalence of LVH was calculated by indexing LVM to both self-reported and measured anthropometric values. In the whole population, LVH tended to be underestimated by self-reported values by 5.4% according to criterion A (48.5% vs. 53.9%, p < 0.001) and by 1.2% according to criterion B (29.6% vs. 30.8%, p < 0.01); similar findings were observed in the hypertensive subgroup encompassing one-half of the sample. Underestimation of LVH was more pronounced in older patients than in younger patients: 8.6% vs. 3.2% (p < 0.001) by criterion A, 3.1% vs. 0.1% (p < 0.001) by criterion B, in women than in men (8.6% vs. 3.3% (p < 0.001) by criterion A and 1.8% vs. 0.5% (p < 0.01) by criterion B. In a sample of outpatients attending echocardiographic laboratories, LVH is misclassified when left ventricular mass is normalized to self-reported weight and height. The error is related to the clinical characteristics of patients and is more pronounced when LVM is normalized to height(2.7).     

Echocardiographic definition of left ventricular hypertrophy in the hypertensive: which method of indexation of left ventricular mass?

OBJECTIVES: It has been suggested that hypertensives at high risk of cardiovascular complications can be identified on the basis of their left ventricular mass as determined echographically. However, there is as yet a lack of consensus on the mode of indexation (body surface area, height, height 2.7) of left ventricular mass (LVM), and on the cut-off values for definition of left ventricular hypertrophy (LVH). The main objective of this study is to test the influence of the different modes of indexation for LVM on the prevalence of LVH in a population of never treated hypertensive patients on the basis of cut-offs for LVM based upon its relationship with ambulatory blood pressure (BP) measurement. METHODS: A population of 363 untreated hypertensives was investigated using a standardised procedure. The men and women were analysed separately. We studied the relationship between mean daytime ambulatory systolic BP and LVM and calculated the LVM cut-off for a BP of 135 mm Hg using three different methods of indexation. On the basis of these criteria, the population was divided into those with and those without LVH. RESULTS: The prevalence of LVH was found to be higher when LVM was indexed to height2.7 (50.4%) or height (50.1%). Prevalence was lowest when LVM was indexed to body surface area (48.2%), which tended to minimise the hypertrophy in obese individuals. Only indexation by height 2.7 fully compensates for relationships between height and ventricular mass in this population. CONCLUSIONS: Indexing LVM to height 2.7 thus appeared to give a more sensitive estimate of LVH by eliminating the influence of growth. Cut-offs of 47 g/m2.7 in women and 53 g/m2.7 in men corresponded to a cardiovascular risk indicated by a daytime systolic BP >/=135 mm Hg.     

Prevalence and determinants of left ventricular hypertrophy in acromegaly: impact of different methods of indexing left ventricular mass

BACKGROUND: Left ventricular hypertrophy (LVH) is the most common cardiac abnormality in acromegaly. Left ventricular mass (LVM) is an important parameter measured to detect LVH, but the relationship with body size should be considered by correcting LVM to body surface area (BSA), height or height2.7. All trials concerning acromegaly have detected LVH on the basis of LVM indexed for BSA, but have been criticized for disregarding the effects of obesity. PATIENTS AND MEASUREMENTS: 97 patients with active acromegaly and a control group of 97 nonacromegalic subjects, were compared for the prevalence of LVH, calculated with different corrections of LVM for BSA, height and height2.7. In addition, we evaluated determinants of LVH in acromegalic group. RESULTS: In controls, the prevalence of LVH, determined by correcting LVM for BSA (10.3%) was significantly lower than correcting by LVM/height (21.6%, P = 0.05) and LVM/height2.7 (33%, P < 0.0001). Similarly, in the acromegalic population the prevalence of LVH was significantly higher when measured by LVM/height (86.6%) or LVM/height2.7 (89.7%), than by LVM/BSA (67%) (P = 0.002 and P < 0.0001, respectively). A lower prevalence of LVH detected by LVM/BSA than LVM/height and LVM/height2.7 has been observed in an acromegalic overweight group, while in patients with normal weight there was no significant differences using different corrections. In acromegalic patients with disease duration of 10 years. By separate multiple regression analyses systolic blood pressure was the only independent determinant of LVM/BSA or LVM/height, while systolic blood pressure and GH levels were both predictors of LVM/height2.7. CONCLUSIONS: LVM indexed for height2.7 appears to be the most appropriate method to identify LVH in acromegaly, particularly in overweight patients and those with shorter disease duration.     

Is there a relationship between left ventricular mass and plasma glucose and lipids independent of body mass index? Results of the Gubbio Study

BACKGROUND AND AIMS: The association between left ventricular (LV) mass (M) and variables described as features of the insulin resistance syndrome, such as obesity and measures o lipid and carbohydrate metabolisms, has been reported in hypertensives. The aim of the present study was to investigate in a large, population based group of non hypertensive people, the prevalence of LV hypertrophy (H) and the relationship of LVM with some of the variables described in the insulin resistance syndrome, independently of obesity. For this reason we investigated the normotensive subjects in the age range 45-54 yrs (n = 435) of the total population of participants in the Gubbio Population Study. METHODS AND RESULTS: Serum lipids, cholesterol (Chol), triglyceride (Tg), HDL cholesterol, fasting blood glucose (FBG), blood pressure (BP), body weight and height were measured and body mass index (BMI) was calculated; LVM was assessed by M-mode echocardiography. Using a normalization criterion not related to body weight (g/m2.7) and the cut-off of 49.2 g/m2.7 for men and 46.7 g/m2.7 for women, LVH was found in 25% of the sample whilst, when LVM was corrected by body surface area (cut-off 116 g/m2 for men and 104 g/m2 for women), the prevalence of LVH was quite lower (10.3%). In the univariate analyses LVMi was closely related to BP, BMI and metabolic variables whilst in the multivariate analysis only BP, BMI, and age were detected as independent predictors of LVMi. When the sample was divided into obese and non-obese subjects on the basis of BMI (cut-off 30 kg/m2), no difference in metabolic variables was seen between subjects with and without LVH within each BMI class. Regarding left ventricular geometry, RWT was positively related to triglycerides and blood glucose and inversely to HDL-chol. CONCLUSIONS: The present study in the middle age normotensive sample of the general population of Gubbio extends to normotensives the relationship between left ventricular mass and metabolic parameters already seen in hypertensives. BMI seems to account for most of the increases in LVM since the prevalence of LVH, which was definitely high when LVM was not normalized to body weight, fell to approximately 4% when the influence of body weight was excluded. Moreover differences in metabolic values between subjects with and without LVH disappeared when the subjects were stratified by BMI. Left ventricular geometry, on the other hand, seems to be related to some metabolic variables.     

Prevalence of left ventricular hypertrophy and carotid thickening in a large selected hypertensive population: impact of different echocardiographic and ultrasonographic diagnostic criteria.

BACKGROUND: Left ventricular hypertrophy (LVH) and increased carotid intima-media thickness (IMT) represent independent risk factors for cardiovascular disease. OBJECTIVE: To evaluate the prevalence of echocardiographic LVH and common carotid artery (CCA) intima-media (IM) thickening by different criteria in a large sample of hypertensive patients referred to our Hypertension Clinic. METHODS: Echocardiograms and ultrasonographic carotid examinations have been performed in 640 consecutive hypertensives referred to our outpatient's hypertension unit. LVH was diagnosed using six different criteria, when left ventricular mass index (LVMI) exceeded (a) 100 g/m2 in women and 120 g/m2 in men, (b) 110 g/m2 in women and 125 g/m2 in men, (c) 110 g/m2 in women and 134 g/m2 in men, (d) 125 g/m2 in both sexes, (e) 47 g/h2.7 in women and 51 g/h2.7 in men, (f) 105 g/h in women and 126 g/h in men. Thickening of CCA IM was identified using three partition values; when IMT was (a) > or =0.8 mm; (b) >0.9 mm: (c) > or = 1.0 mm in both sexes. RESULTS: Echocardiographic and ultrasonographic examinations of sufficient quality to be analysed were obtained in 611 patients (95.2%). Prevalence of LVH ranged from 18.6% (d) to 42.2% (f) and was significantly higher in men than in women by criteria (d) and (e), but slightly higher in women when using criteria (a) and (c). Eccentric hypertrophy was the most frequent type of LVH independently of the criteria used. Prevalence of IM thickening ranged from 14.7% (c) to 44.2% (a). Significant correlations between left ventricular mass (LVM)/body surface area, LVM/height and LVM/height2.7, and carotid IM thickness were found (r=0.41; p <0.0001; r=0.31; p <0.0001; r = 0.30; p <0.0001, respectively). CONCLUSION: The prevalence of LVH and CCA IM thickening in hypertensive patients is markedly dependent on the partition values used to define these markers of target organ damage. Considering the pivotal role of LVH and CCA IM thickening in assessing the global cardiovascular risk profile in hypertensives, improved standardization in defining LVH and carotid IM thickening is needed.     

Prognostic implications of left ventricular hypertrophy defined by the thresholds from the international and Chinese guidelines

To compare the predictive value of mortality between left ventricular hypertrophy (LVH) defined by Chinese thresholds and defined by international guidelines in hypertension individuals and investigate better indexation methods for LVH in Chinese population. We included 2454 community hypertensive patients with Left ventricular mass (LVM) and relative wall thickness. LVM was indexed to body surface area (BSA), height^{2 7} and height ^{1 7}. The outcomes were all-cause and cardiovascular mortality. Cox proportional hazards models were used to explore the association between LVH and the outcomes. C-statistics and time-dependent receiver operating characteristic curve (ROC) was used to evaluate the value of those indicators. During a median follow-up of 49 months (interquartile range 2–54 months), 174 participants (7.1%) died from any cause (n = 174), with 71 died of cardiovascular disease. LVM/BSA defined by the Chinese thresholds was significantly associated with cardiovascular mortality (HR: 1.63; 95%CI: 1.00-2.64). LVM/BSA was significantly associated with all-cause mortality using Chinese thresholds (HR: 1.56; 95%CI: 1.14-2.14) and using Guideline thresholds (HR: 1.52; 95%CI: 1.08-2.15). LVM/Height^1.7 was significantly associated with all-cause mortality using Chinese thresholds (HR: 1.60; 95%CI: 1.17-2.20) and using Guideline thresholds (HR: 1.54; 95%CI: 1.04-2.27). LVM/Height^2.7 was not significantly associated with all-cause mortality. C-statistics indicated that LVM/BSA and LVM/Height^1.7 by Chinese thresholds had better predictive ability for mortality. Time-ROC indicated that only LVM/Height^1.7 defined by Chinese threshold had incremental value for predicting mortality. We found that in community hypertensive populations, race-specific thresholds should be used to classify LV hypertrophy related to mortality risk stratification. LVM/BSA and LVM/Height^1.7 are acceptable normalization method in Chinese hypertension.     

Left ventricular filling abnormalities and obesity-associated hypertension: relationship with overproduction of circulating transforming growth factor beta1

This study has been designed to evaluate the relationship among transforming growth factor beta1 (TGFbeta1) and some measurements of diastolic function in a population of hypertensive subjects with normal left ventricular ejection fraction. We studied 67 hypertensive outpatients who according to their BMI levels were subdivided into three groups: lean (L), overweight (OW) and obese (OB) hypertensives (HT). Circulating TGFbeta1 and M- and B-mode echocardiography was determined. All hypertensives were further subgrouped, according to European Society of Cardiology Guidelines, into two subsets of patients with normal diastolic function or with diastolic dysfunction. Prevalence of left ventricular hypertrophy (LVH) was determined in all the groups. TGFbeta1, left ventricular mass (LVM), LVM/h(2.7), E-wave deceleration time and isovolumic relaxation time (IVRT) were significantly (P < 0.005) higher and E/A velocity ratio was significantly (P < 0.05) lower in OW-HT and OB-HT than in L-HT. Prevalence of LVH was significantly higher (P < 0.03) in group OB-HT than in L-HT. TGFbeta1 (P < 0.004), LVM/h(2.7) (P < 0.001) and prevalence of LVH were (P < 0.01) significantly higher in hypertensives with diastolic dysfunction than hypertensives with normal diastolic function. TGFbeta1 levels were positively correlated with BMI (r = 0.60; P < 0.0001), LVM/h(2.7) (r = 0.28; P < 0.03), IVRT (r = 0.30; P < 0.02) and negatively with E/A ratio (r = -0.38; P < 0.002) in all HT. Multiple regression analysis indicated that TGFbeta1, BMI and IVRT were independently related to E/A ratio explaining 71% of its variability (r = 0.84; P < 0.0001). This relationship was independent of LVH, age and HR suggesting that TGFbeta1 overproduction may be considered a pathophysiological mechanism in the development of left ventricular filling abnormalities in obesity-associated hypertension.     

Increased left ventricular mass index and nocturnal systolic blood pressure in patients with Type 2 diabetes mellitus and microalbuminuria.

AIMS: To compare left ventricular mass (LVM) index and function in patients with Type 2 diabetes mellitus with and without microalbuminuria and to investigate the clinical determinants of left ventricular hypertrophy. METHODS: Echocardiography, electrocardiography and 24-h ambulatory blood pressure monitoring were performed in microalbuminuric (n = 29) and normoalbuminuric (n = 29) patients with Type 2 diabetes and no clinical evidence of heart disease. Groups were individually matched for age, sex and diabetes duration and smoking status. RESULTS: LVM index (62 (34-87) vs. 52 (33-89) g/m2.7, P = 0.04) and LVH prevalence, using two out of three definitions, were greater in patients with microalbuminuria (LVM/height2.7: 72 vs. 59%, P = 0.27, LVM/height: 66 vs. 38%, P = 0.04, LVM/body surface area: 59 vs. 31%, P = 0.03). Night-time systolic blood pressure (126 (99-163) vs. 120 (104-157) mmHg, P = 0.005) and the night/day systolic blood pressure ratio (0.92 (0.08) vs. 0.88 (0.06), P = 0.04) were higher in those with microalbuminuria. Systolic and diastolic function were similar in both groups. Linear regression analyses showed that body mass index (BMI) was significantly related to loge LVM index (R2 = 11.8%, P = 0.005) and a relationship with night/day systolic blood pressure was also suggested (R2 = 4.6%, P = 0.057). CONCLUSIONS: In patients with Type 2 diabetes, LVH is more common and severe in those with microalbuminuria. Its presence may be related to raised night/day systolic blood pressure ratio and is significantly related to BMI. The high prevalence of LVH strengthens the case for echocardiographic screening in Type 2 diabetes to identify high risk patients who might benefit from aggressive cardiovascular risk factor intervention.     

Association between fasting plasma glucose and left ventricular mass and left ventricular hypertrophy over 4 years in a healthy population aged 60 and older

OBJECTIVES: To test the association between fasting glucose level and left ventricular mass (LVM) and left ventricular hypertrophy (LVH) in people aged 60 and older. DESIGN: Population-based prospective study with 4-year follow-up. SETTING: Department of Internal Medicine and Family Medicine, Kaohsiung Medical University (KMU), Chung-Ho Memorial Hospital, and Graduate Institute of Medicine and Public Health, KMU. PARTICIPANTS: Of 1,500 people screened, 105 without symptoms or signs of diabetes mellitus, hypertension, or cardiovascular disease were recruited from senior activity centers in Kaohsiung city. MEASUREMENTS: All received two-dimensional echocardiography and fasting glucose examination at baseline and at 2- and 4-year follow-up. LVH was defined as a LVM index (LVMI) greater than 122.4 g/m(2) or 51 g/m(2.7). RESULTS: Age ranged from 60 to 81 (mean 71.7+/-3.9). Baseline glucose ranged from 83 to 118 mg/dL (mean 99.7+/-7.9 mg/dL). LVMI was significantly higher at the 4-year follow-up (97.5+/-24.9 vs 104.5+/-27.5 g/m(2) and 44.2+/-12.1 vs 47.2+/-13.4 g/m(2.7), both P<.01), as was the occurrence of LVH (16% vs 32% and 25% vs 39%, both P<.01). Baseline glucose correlates with 4-year change in LVMI (both P<.02). In the fourth year, baseline glucose was a significant predictor of LVMI (both P<.01) and LVH (P=.03 in g/m(2) definition) using logistic regression analysis. CONCLUSION: Because fasting glucose is an independent predictor for greater LVM and for development of LVH, it should be considered in assessment of cardiac disease and LVM in healthy older people without diabetes mellitus.     

Excessive increase in left ventricular mass identifies hypertensive subjects with clustered geometric and functional abnormalities

BACKGROUND: Left ventricular mass (LVM) exceeding needs to sustain haemodynamic load has been termed 'inappropriate left ventricular mass'. We hypothesized that inappropriate LVM identifies hypertensive patients with clustered cardiac geometric and functional abnormalities. METHODS: For this purpose, 359 hypertensive individuals without prevalent cardiovascular disease underwent Doppler echocardiography. Observed LVM exceeding more than 28% of the value predicted for individual cardiac work, body size and sex was defined as inappropriate LVM. Concentric left ventricular geometry was defined as age-adjusted relative wall thickness (RWT) greater than 0.40. Systolic dysfunction was defined as ejection fraction less than 50% or midwall shortening less than 14.7%. Diastolic dysfunction was defined as isovolumic relaxation time (IVRT) greater than 100 ms, E-velocity deceleration time greater than 220 ms or age and heart rate-normalized early/late (E/A) ratio less than 0.66. Left ventricular hypertrophy (LVH) was defined as an LVM index greater than 49.2 g/m2.7 in men and 46.7 g/m2.7 in women. RESULTS: As expected, inappropriate LVM was associated with higher RWT, lower left ventricular systolic function, longer IVRT and prolonged E-deceleration time (all P < 0.05). Patients with inappropriate LVM had a higher prevalence of concentric geometry (65.5 versus 40.4%), systolic dysfunction (67.9 versus 47.4%) and diastolic dysfunction (46.4 versus 39%; all P < 0.001) than those with LVH. Inappropriate LVM had greater sensitivity (0.89 versus 0.54) and specificity (0.82 versus 0.62; both P < 0.01) than LVH in identifying patients with clustered left ventricular concentric geometry, systolic and diastolic dysfunction. CONCLUSIONS: Inappropriate LVM is associated with a cluster of concentric left ventricular geometry, delayed left ventricular relaxation and reduced systolic performance. Compared with LVH, inappropriate LVM is more accurate at identifying patients with clustered left ventricular geometric and functional abnormalities.     

Relation between socioeconomic status, race-ethnicity, and left ventricular mass: the Northern Manhattan study

Increased left ventricular mass (LVM) and lower socioeconomic status (SES) are predictors of cardiovascular morbidity and mortality. Blacks and Hispanics are more likely to have higher LVM and lower SES. The relation between SES, race-ethnicity, and LVM has not been fully explored. Data were used from the NOMAS population-based sample of 1916 subjects living in Northern Manhattan. SES was characterized on the basis of educational attainment and divided into 4 categories. Echocardiography-defined LVM was indexed according to height at the allometric power of 2.7 and analyzed as a continuous variable. LVM varied by race in our cohort (blacks 48.9 g/m2.7, Hispanics 48.4 g/m2.7, whites 45.6 g/m2.7; P=0.004). Using ANCOVA, there was a significant inverse and graded association between mean LVM and SES for the total cohort. Mean LVM was 48.4 g/m2.7, 48.6 g/m2.7, 47.1 g/m2.7, and 45.3 g/m2.7 for the lowest to the highest educational level category (P trend=0.0004). This relationship remained among normotensives (P trend=0.0005) and was present for blacks (P trend=0.009), but not for whites (P trend=0.86) or Hispanics (P trend=0.47). The difference in mean LVM between the highest and lowest categories of education was 5.3 g/m2.7 for blacks, 0.0 g/m2.7 for whites, and 1.0 g/m2.7 for Hispanics. Lower SES is an independent predictor of increased LVM among hypertensive and normotensive blacks.     

Cardiac magnetic resonance assessment of left ventricular mass in autosomal dominant polycystic kidney disease

Summary

Background and objectives

Autosomal dominant polycystic kidney disease (ADPKD) is associated with a substantial cardiovascular disease burden including early onset hypertension, intracranial aneurysms, and left ventricular hypertrophy (LVH). A 41% prevalence of LVH has been reported in ADPKD, using echocardiographic assessment of LV mass (LVM). The HALT PKD study was designed to assess the effect of intensive angiotensin blockade on progression of total kidney volume and LVM. Measurements of LVM were performed using cardiac magnetic resonance (MR).

Design, setting, participants, & measurements

Five hundred forty-three hypertensive patients with GFR >60 ml/min per 1.73 m² underwent MR assessment of LVM at baseline. LVM was adjusted for body surface area and expressed as LVM index (LVMI; g/m²).

Results

Baseline BP was 125.1 ± 14.5/79.3 ± 11.6 mmHg. Average duration of hypertension was 5.79 years. Prior use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers was present in 59.5% of patients. The prevalence of LVH assessed using nonindexed LVM (g) was 3.9% (n = 21, eight men and 13 women) and 0.93% (n = 5, one man and four women) using LVMI (g/m²). In exploratory analyses, the prevalence of LVH using LVM indexed to H^2.7, and the allometric index ppLVmass_HW, ranged from 0.74% to 2.23% (n = 4 to 12). Multivariate regression showed significant direct associations of LVMI with systolic BP, serum creatinine, and albuminuria; significant inverse associations with LVMI were found with age and female gender.

Conclusions

The prevalence of LVH in hypertensive ADPKD patients <50 years of age with short duration of hypertension, and prior use of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers is low. Early BP intervention in ADPKD may have decreased LVH and may potentially decrease cardiovascular mortality.     

Left Ventricular Hypertrophy Phenotype in Childhood‐Onset Essential Hypertension

The aim of this study was to determine the risk factors associated with left ventricular (LV) hypertrophy (LVH) among 89 untreated children with primary hypertension. Clinic hypertension was confirmed by 24‐hour ambulatory blood pressure (BP) monitoring. LV mass (LVM) index was calculated as LVM (g)/height (m)^2.7 and LVH was defined as LVM index >95th percentile. Children with (n=32) and without (n=57) LVH were compared. Both obesity and systolic BP were independently associated with LVH, with a higher contribution by body mass index. Obesity contributed significantly, with a nearly nine‐fold increased risk of LVH. There was evidence of effect modification by the presence or absence of obesity on the relationship between systolic BP and LVH, whereby the relationship existed mainly in nonobese rather than obese children. Hence, to achieve reversal of LVH, clinicians should take into account both BP control and weight management.     

Appropriate or inappropriate left ventricular mass in the presence or absence of prognostically adverse left ventricular hypertrophy

OBJECTIVES: To evaluate whether assessment of appropriateness of left ventricular mass (LVM) adds to the traditional definition of left ventricular hypertrophy (LVH). DESIGN: Cross-sectional, relational. METHODS: Echocardiographic LVH and appropriateness of LVM were studied in 562 subjects (231 normotensive controls, aged 35+/-11 years, 142 women; 331 hypertensive patients, aged 47+/-11 years, 135 women) classified on the basis of either the presence or the absence of both LVH (LVM index > or = 51 g/m2.7) and inappropriate LVM (LVM > 128% of the value predicted by an equation including age, sex and stroke work). RESULTS: Body mass index was comparable in hypertensive patients and controls. Hypertensive patients without LVH but with inappropriate LVM (n = 21) had higher relative wall thickness and total peripheral resistance than all other groups, whereas cardiac output was lower (all P < 0.001). Midwall mechanics was normal with appropriate LVM, independently of presence of LVH, whereas it was depressed in inappropriate LVM, either with or without LVH (both P < 0.0001). There was no substantial difference in ejection fraction among controls and hypertensive groups. Stress-corrected midwall shortening was more closely related to deviation of LVM from the value appropriate for stroke work, body size and gender (r = -0.56, P < 0.0001) than to LVM index (r = -0.26). CONCLUSIONS: Inappropriate LVM is associated with concentric geometry, high peripheral resistance and depressed wall mechanics. The deviation of LVM from the value appropriate for stroke work, body size and sex correlates with measures of myocardial function better than LVM.     

Association of fat-free mass and training status with left ventricular size and mass in endurance-trained athletes

OBJECTIVES: We sought to study the relationship between left ventricular (LV) size and body composition in male endurance athletes and age-matched control subjects. BACKGROUND: Endurance training is associated with increases in both left ventricular mass (LVM) and left ventricular end-diastolic dimension (LVEDD) in athletes. In other populations, LVM is independently predicted by fat-free mass (FFM). We hypothesized that the increase in LV size and mass observed with training may be a normal response to increased FFM. METHODS: Twelve young and 18 older male endurance athletes and 10 young and 18 older untrained men underwent exercise testing, echocardiography, and dual-photon x-ray absorptiometry body composition analysis. Univariate correlates (Spearman) and multivariate determinants of LVM and LVEDD were sought from: height, height(1.4), height(2.7), height(3.0), body surface area (BSA), FFM, weight, and body mass index. Un-indexed and indexed LVM and LVEDD were then compared. RESULTS: Athletes were of a similar age, weight, and height, but had higher FFM and maximum oxygen uptake than untrained men. Both LVM and LVEDD were correlated with body size, including FFM, BSA, weight, and height (all p < 0.05). On multivariate analysis, FFM was the only independent predictor of both LVM (R(2) = 0.36, p < 0.001) and LVEDD (R(2) = 0.35, p < 0.001). Furthermore, LVM and LVEDD (un-indexed and indexed to BSA and height) were different between athletes and non-athletes, but not when indexed to height(2.7) or FFM. CONCLUSIONS: Both LVM and LVEDD are predicted by FFM in endurance athletes, and when indexed to FFM, no training-related differences were observed. Thus, the extent of LV remodeling (athletic heart) in trained individuals may reflect a normal physiologic response to increased FFM induced by training.     

Impact of adiponectin on left ventricular mass index in non-complicated obese subjects

To evaluate the relationship between the adiponectin levels and left ventricular mass index (LVMI) in uncomplicated obese subjects. Fifty-nine subjects were assigned to the obese (BMI> or =30 kg/m(2)) and 58 to the lean (BMI<30 kg/m (2) ) group. Plasma glucose, insulin, serum total cholesterol and high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, triglycerides and adiponectin were measured. Insulin resistance was determined by the Homeostasis Assessment Model (HOMA-IR). The left ventricular functions of all subjects were determined by 2D and pulse wave Doppler echocardiography. LVMI was calculated as left ventricular mass (LVM) normalized for height in m (2.7) . The obese group displayed significantly higher LVMI and late mitral inflow velocity. Thirty-three obese subjects met the criteria for left ventricular hypertrophy (LVH) and had lower serum adiponectin levels compared with obese subjects without LVH and lean subjects (p<0.05). Adiponectin was negatively correlated with LVMI (R: -0.277, p: 0.002). Furthermore, during the partial correlation analysis where HOMA-IR was controlled, the negative correlation between adiponectin and LVMI progressed (r: -0.283, p: 0.002). The linear regression analysis showed an independent relationship between LVMI and adiponectin. (beta: -0.214, p: 0.01) Obesity is associated with LVH. This study showed direct influence of adiponectin on LVMI.     

Arterial hypertension,left ventricular geometry and QT dispersion in a middle-aged Estonian female population

The aim of the present study was to determine the prevalence of Left ventricular hypertrophy (LVH) and different left ventricular (LV) geometric patterns in the middle-aged women population of Tallinn, to assess the relationship between LV geometry, age, blood pressure and LV repolarization duration and inhomogeneity. A random sample of the population, 482 women aged 35-59, was examined in the framework of a cardiovascular risk factors survey for the WHO/CINDI programme years 1999-2000. Patients with valvular pathology, primary cardiomyopathy, atrial fibrillation, bundle branch blocks and flat T wave on electrocardiography (ECG) were excluded; 398 (82.2%) of the participants underwent echocardiography (Echo) and standard 12-lead ECG at rest and were included in the study. LVH was defined if left ventricular mass (LVM), LVM/height and LVM/BSA were >198 g, >121 g/m and > 120 g/m2, respectively. Arterial hypertension was determined in 23.1% of the women. The prevalence of arterial hypertension was three times higher in those aged 50-59 than in those aged 40-49 (37.4% vs 13.2%; p < 0.05). Different geometric patterns were found as follows: concentric hypertrophy in 9.1%; eccentric hypertrophy 33.9%; concentric remodelling 9.5% and normal geometry 47.5% of the participants. Concentric hypertrophy was found exclusively in hypertensive women and increased with age. No age-related eccentric hypertrophy and concentric remodelling differences were found, either in the normotensive or in the hypertensive group. Prolonged QT dispersion--a marker of increased myocardial electrical instability, was associated with LVH and arterial hypertension and was related mostly to concentric hypertrophy in hypertensives.     

Relation of various degrees of body mass index in patients with systemic hypertension to left ventricular mass, cardiac output, and peripheral resistance (The Hypertension Genetic Epidemiology Network Study).

The impact of different methods of indexation of left ventricular (LV) mass and systemic hemodynamic variables on prevalences and correlates of cardiovascular abnormalities in relation to level of obesity in populations remains unclear. We evaluated 1,672 participants in the Hypertension Genetic Epidemiology Network Study to investigate the relations of overweight and level of obesity to LV mass and prevalences of LV hypertrophy, abnormal cardiac output, and peripheral resistance detected using different indexations for body size. In our study population, 1,577 subjects were clinically healthy nondiabetic hypertensive and 95 were normotensive normal-weight nondiabetic reference subjects. Fat-free mass (FFM) did not differ between the reference group and the normal-weight hypertensive subjects, and increased with overweight. In hypertensive subjects, LV mass and cardiac output increased and total peripheral resistance decreased with overweight. Indexation of LV mass for FFM or body surface area (BSA) resulted in no difference or even lower prevalence of LV hypertrophy in severely obese compared with normal-weight hypertensive subjects. In contrast, indexation of LV mass for height(2.7) identified an increased prevalence of LV hypertrophy with overweight and obesity. Absolute cardiac output increased and total peripheral resistance decreased with overweight. Prevalence of elevated cardiac output indexed for height(1.83) increased and for elevated total peripheral resistance-height(1.83) index decreased with greater overweight, whereas opposite trends were seen when cardiac output and total peripheral resistance were indexed for BSA or FFM. Thus, in hypertensive subjects, FFM increases with overweight and is directly related to LV mass, stroke volume, and cardiac output, and inversely related to total peripheral resistance. Indexations of LV mass and systemic hemodynamics for FFM or BSA obscured associations of LV hypertrophy and abnormal cardiac and total peripheral resistance indexes with overweight, whereas LV mass/height(2,7), cardiac output/height(1.83), and total peripheral resistance-height(1.83) detected significant preclinical cardiovascular abnormalities with obesity.     

Left ventricular mass and hypertrophy assessment by means of the QRS complex voltage-independent measurements

ECG QRS-complex voltage-based criteria are relatively insensitive for detection of increased left ventricular mass (LVM). We developed and evaluate a new ECG index for LV hypertrophy (LVH) detection regardless of the QRS voltage. METHODS: Study population consisted of 106 patients (73 m, 33 f, aged 60 +/- 10 years) with established coronary artery disease (CAD). All patients had LVM assessed echocardiographically and indexed to BSA (LVMI(ECHO)). LVH was diagnosed if LVMI(ECHO) >117 g/m2 in men and >104 g/m2 in women. LV geometry was also determined. Analysed ECG variables, obtained from 12 leads recorded simultaneously, were: the QRS complex duration (QRSd, ms), the average 12-lead time to maximal deflection (TMD, ms), the average 12-lead QRS complex voltage (12QRSV, mV), the average product of 12 lead QRS voltage and duration (12QRSVd, mV ms), Sokolow-Lyon voltage and V-d product (SLV, SLVd), Cornell voltage and V-d product (CV, CVd). A newly developed index, LVM(ECG), was calculated, as LVM(ECG) = [(2 x TMD+QRSd/pi)3-(QRSd/pi)3]*0.0001 (ms3), and indexed to BSA (LVMI(ECG), ms3/m2). RESULTS: Means of the QRS voltage-related parameters were similar in patients with LVH and normal LVM. Greater differences existed between both groups when the QRS voltage-duration products were compared. LVMI(ECG) was most powerful in distinguishing between groups (130 +/- 33 LVH vs 91 +/- 21 normal LVM, p < 0.001). LVMI(ECG) correlated with LVMI(ECHO) better (r = 0.77, p < 0.001) than other indices (r coefficients between 0.24 for SLV and 0.49 for CVd). None of the examined indices allowed for distinction between eccentric and concentric LVH. The new index showed better statistical performance (area under ROC = 0.861) compared to the other indices (AUC range 0.545-0.697, p<0.001 vs LVMI(ECG)). At the specificity level of 92%, the value of LVMI(ECG) > 120 ms3/m2 had the sensitivity of 64% for detection of increased LVM. The sensitivities of the other parameters were significantly lower (sensitivity range 18-42%). Relative intra- and interobserver errors and correlation coefficients for LVMI(ECG) calculation were 0.4% and 1.6% and r = 0.94 and 0.98, respectively. CONCLUSIONS: In patients with CAD an assessment of LV mass and detection of hypertrophy using the QRS complex time-dependent index is feasible. The new index correlated well with echocardiographically-determined LVM and showed better statistical performance than indices which include QRS-voltage measurements. The results are promising and warrant further studies to evaluate the utility of the new index as a risk predictor.     

Insertion/deletion polymorphism of angiotensin I converting enzyme gene and left ventricular hypertrophy in patients with type 2 diabetes mellitus

INTRODUCTION: Left ventricular hypertrophy (LVH) is a well known risk factor of death from cardiovascular causes. Patients with type 2 diabetes mellitus are at particularly high risk of developing cardiovascular disease, which accounts for 80% of deaths in this group. Type 2 diabetes mellitus is probably related to increased left ventricular mass (LVM). Existing data show that the renin-angiotensin-aldosterone (RAA) system may play a role in the development of LVH. Since the I/D polymorphism of angiotensin-converting enzyme (ACE) gene influences the activity of RAA, it is likely that it could also have an impact on LVH. AIM: To assess the relationship between I/D polymorphism of the ACE gene and the severity of LVH assessed by echocardiography (Echo) in patients with type 2 diabetes mellitus. METHODS: The study group consisted of 103 patients (37 women and 66 men; mean age 60.1+/-9.1 years) suffering from type 2 diabetes mellitus with a mean duration of 9.0+/-6.5 years. BMI, waist-to-hip ratio (WHR), arterial blood pressure, LVM and LVM index (LVM indexed for body surface area [g/m(2)] or height raised to the power 2.7 [g/m(2.7)]) were evaluated. I/D polymorphism of the ACE gene was determined using polymerase chain reaction (PCR). RESULTS: Distribution of I/D polymorphism of the ACE gene in the study group was as follows: genotype II--32.0%, ID--42.7%, DD--25.2% of patients. LVH was diagnosed in 43-71% of patients (depending on criteria used). Distribution of individual genotypes was similar in patients with and without LVH. Genotypes II, ID and DD were observed in 37.3%, 31.4% and 31.4% of patients without LVH (according to the Levy criteria) and in 26.9%, 53.9%, 19.2% in the LVH group, respectively. In persons with DD genotype, when compared to group II, significantly higher values of systolic and diastolic blood pressure were noted (147.7+/-20.2 vs 138.2+/-16.7 mmHg, p=0.03 and 89.4+/-9.7 vs 81.9+/-8.7 mmHg, p=0.004, respectively). CONCLUSIONS: In patients with type 2 diabetes mellitus there is no relationship between I/D polymorphism of the ACE gene and LVH.